Vitamin C alleviates alcoholic liver injury by suppressing neutrophil infiltration in senescence marker protein 30-knockout mice irrespective of its antioxidant effects

Life Sciences ◽  
2021 ◽  
pp. 120228
Author(s):  
Su-Min Baek ◽  
Seoung-Woo Lee ◽  
Young-Jin Lee ◽  
Hee-Yeon Kim ◽  
Min-Soo Seo ◽  
...  
Keyword(s):  
Liver Injury ◽  
Vitamin C ◽  
Knockout Mice ◽  
Neutrophil Infiltration ◽  
Alcoholic Liver Injury ◽  
Marker Protein ◽  
Antioxidant Effects

scholarly journals Animals Models of Gastrointestinal and Liver Diseases. Animal models of alcohol-induced liver disease: pathophysiology, translational relevance, and challenges

2014 ◽  
Vol 306 (10) ◽  
pp. G819-G823 ◽  
Author(s):  
Stephanie Mathews ◽  
Mingjiang Xu ◽  
Hua Wang ◽  
Adeline Bertola ◽  
Bin Gao
Keyword(s):  
Liver Disease ◽  
Liver Injury ◽  
Neutrophil Infiltration ◽  
Alcoholic Liver Injury ◽  
Drinking Patterns ◽  
Excessive Alcohol Consumption ◽  
Ethanol Feeding ◽  
History Of ◽  
Excessive Alcohol ◽  
Binge Ethanol

Over the last four decades, chronic ethanol feeding studies in rodents using either ad libitum feeding or intragastric infusion models have significantly enhanced our understanding of the pathogenesis of alcoholic liver disease (ALD). Recently, we developed a chronic plus binge alcohol feeding model in mice that is similar to the drinking patterns of many alcoholic hepatitis patients: a history of chronic drinking and recent excessive alcohol consumption. Chronic+binge ethanol feeding synergistically induced steatosis, liver injury, and neutrophil infiltration in mice, which may be useful for the study of early alcoholic liver injury and inflammation. Using this chronic+binge model, researchers have begun to identify novel mechanisms that participate in the pathogenesis of alcoholic liver injury, thereby revealing novel therapeutic targets. In this review article, we briefly discuss several mouse models of ALD with a focus on the chronic+binge ethanol feeding model.

scholarly journals Vitamin C Is Not Essential for Carnitine Biosynthesis in Vivo: Verification in Vitamin C-Depleted Senescence Marker Protein-30/Gluconolactonase Knockout Mice

2008 ◽  
Vol 31 (9) ◽  
pp. 1673-1679 ◽  
Author(s):  
Hajime Furusawa ◽  
Yasunori Sato ◽  
Yasukazu Tanaka ◽  
Yoko Inai ◽  
Akiko Amano ◽  
...  
Keyword(s):  
Vitamin C ◽  
Knockout Mice ◽  
Marker Protein

scholarly journals Pancreatic insulin release in vitamin C-deficient senescence marker protein-30/gluconolactonase knockout mice

2012 ◽  
Vol 50 (2) ◽  
pp. 114-118 ◽  
Author(s):  
Takafumi Senmaru ◽  
Masahiro Yamazaki ◽  
Hiroshi Okada ◽  
Mai Asano ◽  
Michiaki Fukui ◽  
...  
Keyword(s):  
Vitamin C ◽  
Insulin Release ◽  
Knockout Mice ◽  
Marker Protein ◽  
Pancreatic Insulin

scholarly journals High dietary vitamin C intake reduces glucocorticoid-induced immunosuppression and measures of oxidative stress in vitamin C-deficient senescence marker protein 30 knockout mice

2019 ◽  
Vol 122 (10) ◽  
pp. 1120-1129 ◽  
Author(s):  
Ryusei Uchio ◽  
Yoshitaka Hirose ◽  
Shinji Murosaki ◽  
Akihito Ishigami
Keyword(s):  
Antioxidant Activity ◽  
Ascorbic Acid ◽  
T Cell ◽  
Vitamin C ◽  
Knockout Mice ◽  
The Other ◽  
Dietary Vitamin ◽  
Marker Protein ◽  
Wild Type ◽  
Plasma Ascorbic Acid

AbstractVitamin C (VC) is a vital micronutrient for humans and some other mammals and also has antioxidant activity. Stress-induced elevation of glucocorticoid production is well known to cause immunosuppression. The present study evaluated the effect of high VC intake on glucocorticoid-induced immune changes in mice. Senescence marker protein 30 knockout mice with genetic VC deficiency were fed a diet containing the recommended VC content (20 mg/kg per d; 0·02 %VC group) or a high VC content (200 mg/kg per d; 0·2 %VC group) for 2 months, then dexamethasone was given by intraperitoneal injection. After administration of dexamethasone, the plasma ascorbic acid concentration decreased significantly in the 0·02 %VC group and was unchanged in wild-type C57BL/6 mice on a VC-deficient diet (wild-type group), while it was significantly higher in the 0·2 %VC group compared with the other two groups. In the 0·02 %VC and wild-type groups, dexamethasone caused a significant decrease in the cluster of differentiation (CD)4+ and CD8+ T cells among splenocytes as well as a significant decrease in IL-2, IL-12p40 and interferon-γ protein production by splenocytes and a significant decrease in T-cell proliferation among splenocytes. In the 0·2 %VC group, these dexamethasone-induced immunosuppression improved when compared with the other two groups. In addition, reduction in the intracellular levels of ascorbic acid, superoxide dismutase and glutathione in splenocytes by dexamethasone as well as elevation in thiobarbituric acid-reactive substances were significantly suppressed in the 0·2 %VC group. These findings suggest that high dietary VC intake reduces glucocorticoid-induced T-cell dysfunction by maintaining intracellular antioxidant activity.

Characterization of Endothelial Dysfunction in Microrna-34A Knockout Mice with Alcoholic Liver Injury

2017 ◽  
Vol 152 (5) ◽  
pp. S1111
Author(s):  
Ying Wan ◽  
Kelly M. McDaniel ◽  
Nan Wu ◽  
Sugeily Ramos-Lorenzo ◽  
Tianhao Zhou ◽  
...  
Keyword(s):  
Endothelial Dysfunction ◽  
Liver Injury ◽  
Knockout Mice ◽  
Alcoholic Liver Injury
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